|Feature type||allele||Associated gene||Dmel\hop|
|Also Known As||hopC111|
|Allele class||loss of function allele, amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Deletion of about 300bp of genomic DNA.
|Phenotype Manifest In|
40% of embryos from hop germ line clones show germ-band extension defects. Hemizygous hop mutant germ-band epithelial cells are normal in the head and dorsal-most regions of the embryo, however intercalating (ventrolateral) cells show a smaller apical cell surface.
The proventriculus development is normal in early stages of proventriculus development in mutants. However in the keyhole stage, the anterior boundary cells fail to move inward into the endodermal keyhole domain and arrest anterior to the proventricular endoderm until late stages of embryonic development. Furthermore, the endodermal cell layer of the keyhole is disorganised and the proventriculus is collapsed.
Paternally rescued hop2 germ-line clone embryos are missing denticle belt A5 and part of A4. In the absence of paternal rescue, more severe segmentation defects are seen. Paternally rescued hop2 germ-line clone embryos have defective tracheal systems, generally having several disruptions in the main trunk and several branches.
Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic hop function) have incompletely elongated hindguts which are wider than normal. There are a greater number of cells in the circumference of the mutant hindgut than in wild type. The total number of hindgut epithelial cells is 89% of wild type.
The number of pole cells in embryos derived from hop2 female germ line clones is not different to the number in wild-type embryos. However, in late stage embryos these pole cells fail to coalesce and/or form gonads.
hop25/hop2 egg chambers lack border follicle cells and have reduced numbers of stretched (nurse) follicle cells and posterior polar follicle cells, but increased numbers of main body (oocyte) follicle cells. Nurse follicle cell and centripetally migrating follicle cell domains are shifted posteriorly. When presumptive border cells are mutant for hop2 they fail to express markers of differentiation, and are delayed in migration. When follicle cells overlying the nurse cells are mutant for hop2 they fail to stretch at stage 9 as wild-type nurse follicle cells do, or to express nurse follicle cell markers.
Homozygous mutant border cells, made as somatic clones, fail to migrate. Occasionally a mutant border cell cluster is displaced quite far from the anterior tip of the egg chamber and is associated with abnormally shaped mutant stretch cells.
Paternally rescued embryos derived from females containing homozygous germ-line clones lack abdominal segment 5 and part of abdominal segment 4. These embryos form a defective tracheal system with several disruptions in the main trunk and many branches.
Mosaic egg chambers which are homozygous for hop2 in the germline (but not in the soma) are not fused and all contain 15 nurse cells and one oocyte.
When homozygous somatic clones are made in the egg chamber, defects in border cell migration are seen. Whenever the polar cells are mutant, a complete failure in border cell migration is seen. However, in egg chambers in which the germ-line is mutant, no migration defect is seen. Nor are border cell defects seen when large clones are made in the rest of the follicle cell epithelium. In mutant egg chambers outer border cell clusters consist of an average of 2.1 cells, as compared to 6 in wild-type.
Mutant adult testes contain hub cells but lack stem cells and spermatogonia. A few spermatocytes and terminal epithelial cells remain.
hop2 somatic clones in the eye are rare and have a cell autonomous growth disadvantage when compared to their wildtype twins. They occasionally have missing photoreceptor cells and polarity defects. In the rare larger clones a striking cell non-autonomous effect is seen. Ommatidia at the polar margin of the clones reverse their polarity such that the ommatidia point away rather than toward the equator, thus creating an ectopic equator. When a clone is observed very close to the dorso-ventral midline, the equator was deflected away and formed along the border of the clone. Most of the ommatidia with reversed polarity were composed entirely of wild-type photoreceptor cells. This effect was seen in both dorsal and ventral halves of the eye.
Homozygous clones in the eye show a regular array of ommatidia which contain the wild-type complement of correctly differentiated and positioned photoreceptor cells within the ommatidia. A large proportion of homozygous clones in the eye result in polarity defects in which ommatidia straddling the polar boundary of the clone show inverted dorsoventral polarity. The phenotype is strongest in larger clones and in clones in which the polar boundary runs parallel to the equator of the eye. Typically, one or two rows of ommatidia are inverted, with the strongest phenotype seen having about five inverted rows. Both totally mutant ommatidia adjacent to the polar boundary of the clone and mosaic ommatidia at the clonal border can assume an inverted fate, and occasionally, an ommatidial cluster immediately outside the clone in which all the photoreceptors are wild type is seen to have inverted polarity. Mutant ommatidia in the centre of the clone and on the equatorial margin of the clone show normal orientation. This phenotype is seen in both adults and third larval instar imaginal discs.
hop2 embryos derived from homozygous female germ line clones show loss of the fifth abdominal denticle band and the posterior mid-ventral portion of the fourth band. Variable reduction of the second thoracic and eighth abdominal denticle bands and variable fusion of the sixth and seventh denticle bands is seen.
Maternal effect segmentation phenotype is similar to that caused by loss of Stat92E activity during embryogenesis. Both paternally rescued and unrescued embryos show a consistent deletion of the fifth abdominal segment and the posterior midventral portion of the fourth abdominal segment. Additional defects are seen in the head and tail of the unrescued embryos.
Larval diploid imaginal tissues are reduced in size. Embryos derived from females lacking hop die with characteristic segmentation defects, deletion of the fifth abdominal denticle belt and posterior mid-ventral portion of the fourth abdominal denticle belt.
Paternal rescue of the maternal effect. Germline clone analysis demonstrates that embryos have one abdominal segment missing and A4 appears wider than wild type, and partial or complete fusion of T1 and T2.
hop2/hop[+] is a suppressor | partially of visible phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, osScer\UAS.cCa
|Phenotype Manifest In|
hop2 has abdominal 4 ventral denticle belt | germline clone | maternal effect phenotype, suppressible by Cdk4hs.PC
hop2 has abdominal 4 ventral denticle belt | germline clone | maternal effect phenotype, suppressible by CycEhs.PO
hop2 has abdominal 5 ventral denticle belt | germline clone | maternal effect phenotype, suppressible by Cdk4hs.PC
hop2/hop[+] is an enhancer of wing vein | ectopic phenotype of Scer\GAL4en-e16E, Socs44AScer\UAS.cRa
hop2/hop[+] is a suppressor | partially of eye phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, osScer\UAS.cCa
hop2/hop[+] is a suppressor | partially of ommatidium | supernumerary phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, osScer\UAS.cCa
|NOT Suppressor of|
The melanotic tumour phenotype caused by expression of gcm[DN.Scer\UAS.T:en-Rep] under the control of Scer\GAL4[srp.D.cCa] (the animals also carry Scer\GAL80[ts.αTub84B] which has been inactivated by shifting to the restrictive temperature) is completely suppressed in a hop/Y background.
The ectopic wing vein and arching of wing vein L3 phenotypes caused by expression of Socs44A[Scer\UAS.cRa] under the control of Scer\GAL4[en-e16E] are enhanced by hop/+.
The enlarged eye phenotype seen in flies carrying one copy of osGMR.PB is moderately suppressed by one copy of hop2.
The loss of denticle belt A5 and gap in denticle belt A4 seen in hop2 germ-line clone embryos is suppressed by Cdk4hs.PC, or CycEhs.PO, although in both cases the two rescued denticle belts tend to fuse with each other laterally.
Expression of Socs36EAct5C.T:Ivir\HA1 under the control of Scer\GAL4en-e16E in a hop2/+ background induces ectopic vein formation in 17-26% of wings and the size and penetrance of the humeral outgrowth phenotype is increased.
|Complementation & Rescue Data|
|Stocks ( 2 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 7 )|
(Baeg et al., 2005, Callus and Mathey-Prevot, 2002, Li et al., 2003, Josten et al., 2004, Li et al., 2003, Bach et al., 2003, Chen et al., 2003, Johansen et al., 2003, Ghiglione et al., 2002, Li et al., 2002, Beccari et al., 2002, Silver and Montell, 2001, Luo et al., 1999, Hou et al., 1996, Binari and Perrimon, 1994, Hanratty and Dearolf, 1993, Watson et al., 1991, Bertet et al., 2009, Sotillos et al., 2010)
|Secondary FlyBase IDs|
|References ( 35 )|
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|Recent research papers (0)|
|All research papers listed in FlyBase were published before 2011|